To our knowledge, this is the first study to investigate the neural, somatosensory and psychologic correlates of dissociative states in patients with BPD. We used a script-driven imagery method to induce dissociative states during fMRI scanning, and we assessed dissociative psychopathology and pain sensitivity. Dissociative states were characterized by significantly elevated levels of depersonalization, derealization and subjectively reduced sensory perception. We found that BOLD signals were significantly increased in the left inferior frontal gyrus during the presentation of a dissociation-inducing script as compared with a neutral script. Regression analyses revealed positive correlations between BOLD signal and dissociative psychopathology in the left superior frontal gyrus and negative correlations in the right middle and inferior temporal gyrus. In the subgroup of 10 participants with co-morbid PTSD, we also found increased activity in the left cingulate gyrus during induced dissociation, a positive correlation between dissociation scores and activity in the right insula and a negative correlation between dissociation scores and activation in the right parahippocampal gyrus.
Our hypotheses about psychometrically assessed dissociation were confirmed, suggesting that the induction of dissociative states by use of autobiographical script-driven imagery is possible in patients with BPD. We found no difference in the vividness of the recalled experiences, which supports the assumption that differences in the psychometric assessments were not because of a lower ability to imagine the situation or because of avoidance of the dissociative experience. Nevertheless, the requirement of a minimum of attention and readiness to answer the questions during the experiment may provide an explanation as to why the relatively moderate intensities of dissociation (mean 3.0) during the presentation of the dissociation-inducing script were not as high as the retrospectively assessed values of the real situations (mean 7.4). Also, the artificial environment of the scanner may have prevented the development of full-blown dissociative states. Another explanation might be that patients overestimated the intensity of dissociation in the real situation. Because we did not assess heart rate or skin conductance, we do not have additional physiologic markers of hyper- or hypoarousal.
Our results in terms of pain perception in BPD support previous findings that pain perception was lower during states of intense aversive tension than during baseline conditions,30
as well as previously reported correlations between pain perception and aversive inner tension and between pain perception and dissociation.19
Furthermore, the current study provides strong evidence that reduced pain sensitivity is a somatic marker of dissociative states in patients with BPD.
Our findings of increased BOLD signal during dissociative states in the inferior frontal gyrus are in agreement with those of Lanius and coworkers.16
However, in contrast with their results, we observed inferior frontal gyrus activation in the left cerebrum.
Regression analyses revealed a positive correlation between BOLD signal and the intensity of the dissociative experience during presentation of the dissociation-inducing script in the left superior frontal gyrus (BA 6). We found negative correlations in the right middle and inferior temporal gyrus. Regression analyses of BOLD signal and aversive inner tension revealed no significant results, suggesting that the results are related to dissociation rather than to states of inner tension.
The inverse correlations between temporal areas and the intensity of dissociation are in agreement with the corticolimbic model of dissociation that postulates a corticolimbic disconnection in patients with depersonalization disorder.31,32
Röeder and colleagues33
found reduced amygdala activity during induced depersonalization in healthy control participants. Taken together, these findings suggest that reduced temporal activity is a potential correlate of dissociation and reduced pain sensitivity. Despite these correlative results and the reduced pain sensitivity during presentation of the dissociation-inducing script, we did not find any deactivation of the amygdala. One explanation might be the relatively moderate intensity of dissociation as mentioned above.
When we included data from only the participants with BPD and PTSD, we found significantly increased BOLD signal in the left inferior and superior frontal gyrus, right insula and left anterior cingulate gyrus. The activation patterns in this group resembled those from earlier studies involving PTSD patients; these studies also found activation of the inferior frontal gyrus and dorsal cingulate gyrus.16
Interestingly, Lanius and colleagues34
showed that, in patients with dissociative PTSD, thalamic activity was positively correlated with activity in the right insula. Because the insula plays an important role in monitoring internal states,35
increased insula activity during dissociative states may be a correlate of an attentional shift from external to internal foci. Increased cingulate activity has been suggested to resemble a super-suppression of affective arousal during dissociative states.36
Positive correlations between the intensity of dissociation and activation of the left medial frontal gyrus as found in our study are consistent with the corticolimbic model of depersonalization.15
This model postulates that the medial frontal regions inhibit limbic structures during states of depersonalization. Also, in agreement with this model, we found a negative correlation between dissociation and activation in the right parahippocampal gyrus. This is also in keeping with deactivation of the right parahippocampal gyrus in patients with dissociative PTSD.16
In contrast, Felmingham and coworkers17
found a significant positive correlation between dissociative responses and activation in the left parahippocampal gyrus during nonconscious fear in patients with PTSD. Our results are consistent with previous findings;16,17
nevertheless, there are differences in hemispheres or contrary correlations that might result from the different patient sample, the fact that we did not use explicit trauma scripts to induce dissociation, or the different study design (e.g., compared with Felmingham and colleagues17
). The fact that we did not use explicit trauma scripts in our study may be seen as an advantage because our findings are not confounded by the effects of traumatic remembrance. Another strength of our study is the concurrent assessment of dissociative psychopathology and pain sensitivity.
A main limitation of our study is that we did not include a control group. Therefore, it is possible that our results instead reflect the neural correlates of non–borderline specific dissociation states or the neural correlates of emotionally stressful or “loaded” memories. The fact that the regression analyses of BOLD signal and aversive inner tension revealed no significant differences suggests that the results are related to dissociation rather than to aversive inner tension or stress. Also, in the case of tension effects, we would expect a different activation pattern with decreased prefrontal and increased medial temporal activity. Nevertheless, the comparison of the results with a control group would have been useful.
Second, we have reported all results at an uncorrected level of p ≤ 0.001, which weakens the robustness of the data. We emphasize that this was a first attempt to assess neural correlates of dissociation in patients with BPD using the script-driven imagery method; the results of this study may help to design further studies on this topic. A further limitation is the sample size, particularly the number of patients with BPD but not PTSD. This group of 5 patients was too small to conduct a subgroup comparison, which might have revealed more specific reaction and neural activation patterns. The small sample size of 10 patients with PTSD may have prevented detection of further differences.
We used the same order of scripts (neutral script followed by the dissociation-inducing script) for each participant. This was done to prevent carry-over effects from dissociation induction to the neutral scripts, but it may have led to order effects. Furthermore, we did not assess any additional physiologic markers that may have given more insight into the psychophysiology of dissociation. Finally, we did not assess the awareness of fear, which appears to play a crucial role in the activation pattern of dissociation.17
Future studies should examine whether the enhanced activation in frontal regions is a correlate of a control mechanism following the presentation of the script or a neural reflection of dissociation.